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MSII Microbiology > Unit 2 - Bacterial Infections of the Mouth and Pharynx > Flashcards

Unit 2 - Bacterial Infections of the Mouth and Pharynx Flashcards

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Biology 101 flashcards
1
Q

what are viral causes of pharyngitis?

A

Epstein-Barr virus
Adenoviruses
Herpes simplex virus type 1
Coxackie virus

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2
Q

what are fungal causes of pharyngitis?

A

Candida albicans

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3
Q

what are bacterial causes of pharnygitis?

A

Streptococcus pyogenes
Corynebacterium diphtheriae
Neisseria gonorrhoeae

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4
Q

what does pharyngitis examination typically reveal?

A
  • inflammation of pharynx, tonsils, uvula, with exudate
  • cervical lymphadenopathy
  • fever
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5
Q

what percentage of pharyngitis are caused by group A streptococci? which one specifically?

A

30% Streptococcus pyogenes

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6
Q

bacteriology of group A streptococci?

A

beta-hemolytic (complete clear hemolysis)

  • G+ (like all streptococci)
  • bacitracin sensitive
  • cocci grow in chains
  • react with Lancefield group A antiserum
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7
Q

what are virulence factors of group A streptococci? what do they cause?

A
  • pili (attachment)
  • streptokinase (tissue lysis)
  • streptodornase (digests DNA)
  • hyaluronidase (digests CT)
  • pyrogenic toxin (fever, super Ag, toxic shock)
  • erythrogenic toxin (skin rash)
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8
Q

how does one diagnose pharyngitis from group A streptococci?

A

suggested by family or social history

  • rapid Ag detection assays can identify, but prone to false negative results
  • swab, culture, bacitracin sensitive, and G+ is accurate but slow
  • NOT direct examination of smear, as can look identical to other things
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9
Q

what is the reservoir from group A streptococci? transmission?

A

Streptococcus pyogenes is carried in pharynx and skin

  • carriers not symptomatic, but can still infect others
  • transmit via contact or saliva
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10
Q

what are hemolysins in relation to group A strep? which one is diagnostically useful?

A

not virulence factors, but can identify streptococci b/c produce hemolysis on blood agar plates

  • streptolysin O is highly antigenic, inducing short-lived IgM Ab which is diagnostically useful
  • other toxins explain pathogenesis of infections
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11
Q

what are group A strep sensitive to?

A

penicillin, erythromycin, cephalosporins, and bacitracin

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12
Q

what are complications of streptococcal pharyngitis?

A
  • tonsillitis
  • middle ear infections
  • mastoiditis
  • meningitis
  • scarlet fever
  • rheumatic fever

*generally from orpharynx

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13
Q

explain types of tonsillitis from group A strep

A
  • peritonsillar abscess (may need inscision to get pus out)

- Ludwig’s angina (spreads under tongue and swells such that it’s hard to breathe due to asphyxia)

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14
Q

what happens in ear infections from group A strep?

A

occurs in middle ear (also caused by S. pneumoniae or H. influenxa)

  • may be permanent if eustacian tube closes off
  • may be able to spread up to mastoids (mastoiditis)
  • treat with Grommet tube to drain middle ear
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15
Q

how does mastoiditis from group A strep come about?

A

if recurrent middle ear infections occur

-can swell behind ear such that one sticks out

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16
Q

explain meningitis due to group A strep?

A

occurs if bacteria spread from middle ear infection or mastoiditis
-also caused by N. meningitides and S. pneumoniae

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17
Q

explain scarlet fever due to group A strep?

A

due to exotoxin encoded by bacteriophage that carries gene for erythrogenic toxin

  • skin and tongue rash (strawberry tongue)
  • they go away when the sore throat is gone, and not effectively treated by cream
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18
Q

explain rheumatic fever etiology due to group A strep?

A

most serious complication of sore throats

  • post-streptococcal condition that arises around 3 weeks after resolution of group A (M3/5/13 strains)
  • autoimmune condition with fever, polyarthritis, and inflammation of heart leading to permanent deformation (endocarditis; lesions are sterile)
  • children 6-15 are at risk
  • recurrences are common, and patients may need future prophylactic Ab for dentistry and minor surgical procedures
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19
Q

what can prevent group A strep infection?

A

no vaccines, despite many potent Ag

  • prophylactic Ab fro patients who had post-streptococcal diseases
  • treatment of carriers not recommended
  • tonsillectomy reduces risk of future infections in some studies
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20
Q

how do you treat group A strep?

A

not essential, as the infection is self-limiting

  • antibiotics can shorten symptoms by 16 hours and reduce complications
  • systemic penicillin G, amoxicillin, erythromycin, or cephalosporins are suitable
  • drug resistance is not a serious problem
  • patients with a history of rheumatic fever need special attention
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21
Q

what are clinical features of rheumatic fever from group a strep?

A
  • fever
  • polyarthritis
  • heart murmur (vasculitis, myocarditis, endarteritis, Aschoff body)
  • Sydenham’s chorea (rare)
  • duration can be several weeks or months
  • case fatality rate is 2-5%
22
Q

how is the diagnosis of rheumatic fever made?

A

clinical features plus presence of IgM anti-streptolysin O Ab

  • heart lesions and inflammed joints are sterile
  • there is no bacteremia
23
Q

explain the pathogenesis of rheumatic fever?

A

autoimmune with certain M-proteins (M3/5) - although immune pathogenesis hasn’t been demonstrated directly
-certain HLA types are more common in patients than background population

24
Q

rheumatic fever prevalence?

A
  • prevalence has been reducing gradually over last 60+ years
  • rheumatic fever once a compliccation of ~3% streptococcal sore throats, now 0.3%
  • incidence is 50% in patients with a prior attack
25
Q

how can rheumatic fever carditis resolve?

A

resolves with fibrosis of endocardium, or calicification, often with permanent valve distortion
-patients are at life-long risk of endocarditis, and may need antibiotics at times of likely bacteremia (dental extractions)

26
Q

treatment of rheumatic fever?

A

anti-inflammatory drugs (aspirin, steroids)

  • no antibacterial therapy is indicated
  • later, replacement of heart valves may be necessary
27
Q

prevention of rheumatic fever?

A

if have history of it, should use aggressive anti-bacterial therapy in the event of later streptococcal infections

28
Q

explain bacteriology of Streptocccus viridans?

A

(includes S. sanguis and S. mutans)

-alpha-hemolytic (partial hemolysis), optochin-resistant, G+, catalase -

29
Q

what are virulence factors of S. viridans?

A

sugar-metabolizing enzymes and extracellular polysaccharides

-turns LMW sugars to HMW sugars (dental plaque due to biofilms) or acids (demineralization)

30
Q

how does one diagnose dental carries?

A

six-montly dental examinations show early demineralization

-lab testing not informative since bacteria are part of normal flora of mouth in 100% of people

31
Q

what are complications of dental carries?

A

pupitis, abscesses, and cellulitis

-bacteremia and endocarditis may follow dental treatment of susceptible patients

32
Q

how does one treat dental carries?

A

dental treatment to remove decalcified tissue
-acute abscesses can be treated temporarily with penicillin, erythromycin, or cephalosporins are of limited value, but dental extraction is more effective

33
Q

what percent chance to people have of getting S. viridans bacteremia if the undergo…

  1. extraction of first 4 premolars
  2. single extraction
  3. polishing teeth
  4. palcing bands
  5. adjusting bands?
A
  1. 51%
  2. 38.5%
  3. 24.5%
  4. 10%
  5. 0%
34
Q

explain the etiology of endocarditis?

A

previous rheumatic fever causes distortion of endothelium in heart, leading to turbulent blood flow

  • sticky bacteria that come into contact with distorted endothelium can attach and replicate
  • infection can be very persistent
  • damage to heart may be continuous
  • valves are particularly susceptible
35
Q

explain treatment of endocarditis?

A

prolonged antibiotics

  • replacement of heart valves carries risk of new valve becoming infected
  • 50% of patients die despite treatment
36
Q

what are heart vegetations foci of? what do antibiotics do?

A

infection and/or metastatic disease

  • valves are gradually destroyed
  • antibiotics don’t penetrate vegetation
37
Q

what are causes of endocarditis?

A
  • usually caused by S. viridans
  • drug abusers or infected IV lines have S. aureus
  • HACEK group of G- rods
38
Q

how do you make a diagnosis of endocarditis?

A

variable clinical features, confirmed by cardiac examination

  • satellite infectious foci (splinter hemorrhages) under fingernails and in conjunctiva due to release of infected material into circulation
  • blood culture may be positive for causative organisms
39
Q

how does one prevent endocarditis?

A

antibiotic coverage of dental treatment, catheterization in at-risk patients
-bacteremia should be prevented by prophylactic Ab at the time of dental treatment, following current guidelines of AHA

40
Q

explain what periodontal disease is

A

chronic inflammation in oral tissues that are in contact with dental plaque

  • over years, gingiva detaches from tooth, creating a pocket for microorganism proliferation
  • as pocket gets deeper, alveolar bone is destroyed, and mature plaques become calcified
  • eventually teeth loosen and are lost
41
Q

what is “gingivitis” referring to?

A

early stage periodontal disease

-is reversible if dental hygiene is improved

42
Q

what is the cause of periodontal disease?

A

no specific microorganism is responsible, but it’s a mix of anaerobic organisms (mostly G-)
-these organisms are present in small numbers in all people

43
Q

what is treatment for periodontal disease?

A 
dental hygiene (including regular dental scaling to remove calcified plaque)
-periodontal surgery can reduce or eliminate pockets
44
Q

what is the etiology of diphtheria?

A

infection of pharyngeal mucous membrane causing necrosis and pseudomembrane with respiratory obstruction

  • release of toxin causes systemic muscle paralysis, including myocarditis and death in 10-20% of cases
  • mostly a childhood condition
45
Q

what is the bacteria that causes diphtheria?

A

Corynebacterium diphtheriae

  • G+ club-shaped rods
  • metachromatic granules (internal beads)
  • stains may be toxigenic (or not); diphtheroids
  • inhabit skin and mucus membranes, although carriage may be asymptomatic
46
Q

what are virulence factors of Corynebacterium diphtheriae?

A

diptheria toxin encoded by bacteriophage

-causes local and cardiac necrosis

47
Q

what is a “pseudomembrane”?

A

necrotic coagulum of bacteria, epithelial cells, fibrin, leukocytes, erythrocytes forming a gray-brown “pseudomembrane” covering the oro-pharynx

48
Q

how does one diagnose diphtheria?

A
  1. swab nose and throat, beneath pseudomembrane
  2. culture requires tellurite media for C. diphtheria (alert lab)
    - confirm toxin production via Ab tests
  3. PCR confirmation of tox gene

*examination of smears is not useful due to existance of non-pathogenic Corynebacteria (diphtheroids)

49
Q

what is diphtheria treatment?

A

(equine) antitoxin given as soon as possible
- penicillin or erythromycin helps resolution
- mechanical ventilation as needed

50
Q

prevention of dihtheria?

A
  1. childhood vaccination with toxoid (DTaP)
  2. boosters after 1 yr, 5 yr
  3. boosters for adults when traveling to endemic areas (now rare in western world)
51
Q

does bacteremia occur from rheumatic fever, bacterial endocarditis, periodontal disease, and/or dental extraction?

A

from bacterial endocarditis and dental extraction

52
Q

how is diphtheria transmitted?

A

air-borne droplets

MSII Microbiology (23 decks)

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